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Salmonella infection-induced non-responsiveness of murine splenic T-lymphocytes to interleukin-2 (IL-2) involves inhibition of IL-2 receptor gamma chain expression.

作者信息

Matsui K, Arai T

机构信息

Department of Microbiology, Meiji College of Pharmacy, Tokyo, Japan.

出版信息

FEMS Immunol Med Microbiol. 1998 Mar;20(3):175-80. doi: 10.1111/j.1574-695X.1998.tb01125.x.

Abstract

In a previous study we demonstrated that Salmonella typhimurium-induced immunosuppression involved T-cell non-responsiveness to interleukin-2 (IL-2). In this study we observed that Salmonella-induced T-cell non-responsiveness to IL-2 was not reversed completely by treatment with N(G)-monomethyl-L-arginine, which is known to inhibit nitric oxide (NO) secretion by macrophages in culture. Furthermore, when purified splenic T-lymphocytes from Salmonella-infected mice were activated with an anti-CD3 antibody, the responsiveness of these T-cells to IL-2 was suppressed significantly. Results of flow cytometric analysis using an anti-IL-2 receptor gamma chain (IL-2Rgamma) antibody showed that IL-2Rgamma expression in mitogen-activated T-cells was down-regulated by Salmonella infection. These results suggest that Salmonella infection-induced T-cell non-responsiveness to IL-2 involves a defective function of T-cells themselves and appears to be regulated by inhibition of IL-2Rgamma expression in T-cells.

摘要

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